Some inherited degenerative diseases affecting rods and cones irreversibly impair photoreception while leaving the rest of the optical pathway intact. Attempts to restore sight to affected individuals through microchips, gene therapy and even stem cells have had some clinical successes but all pose technical challenges. Now Polosukhina et al. demonstrate how a small-molecule photoswitch can restore vision in mutant mice lacking rods and cones. Injecting acrylamide-azobenzene-quaternary ammonium (AAQ), a light-activatable K+ channel blocker, into the vitreous humor restores pupillary light reflex and light avoidance behavior in blind mice (homozygous for a mutation in cGMP phosphodiesterase-6, causing rods and cones to degenerate by three months of age). AAQ-mediated responses are rapid (median latency of 45 ms), have high spatial resolution (with a field size of 100 mm), and although short wavelength light was most effective, some response was achieved with longer (up to 500 nm) wavelengths. Although AAQ and related molecules may be therapeutic in humans, several issues need addressing. The molecule will need to be modified such that responses can be achieved at appropriate light intensities and wavelengths for the human eye. In addition, as AAQ dissipates within 24 hours, an extended release formulation would be preferred over repeated injections in the eye. (Neuron 75, 271–282, 2012)